Comparison of vessel dilator and long-acting natriuretic peptide in the treatment of congestive heart failure

Vesely, David L.; Dietz, John R.; Parks, James R.; Antwi, Ernest A.; Overton, Rose M.; McCormick, Michael; Cintrón, Guillermo; Schocken, Douglas D.

doi:10.1016/s0002-8703(99)70175-4

Cited by 17 publications

(29 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The best known members of this family are atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), both secreted by the heart, and C-type natriuretic peptide (CNP), which is secreted by the endothelium [25]. These peptides represent less than 5% of the total amount of circulating peptides: the great majority (95%) of peptides are the less familiar, long-acting natriuretic peptide (LANP), vessel dilator and kaliuretic peptide [26].…”

Section: Pgc Pathways and Nps: Nesiritide And Urodilatin/ Ularitidementioning

confidence: 99%

Role of guanylate cyclase modulators in decompensated heart failure

et al. 2009

View full text Add to dashboard Cite

In this review we investigate the role of particulate and soluble guanylate cyclase (pGC and sGC, respectively) pathways in heart failure, and several novel drugs that modify guanylate cyclase. Nesiritide and ularitide/urodilatin are natriuretic peptides with vasodilating, natriuretic and diuretic effects, acting on pGC, whilst cinaciguat (BAY 58-2667) is a novel sGC activator. Cinaciguat has a promising and novel mode of action because it can stimulate cyclic guanosine-3',5'-monophosphate synthesis by targeting sGC in its nitric oxide-insensitive, oxidised ferric (Fe(3+)) or haem-free state. Thus, cinaciguat may also be effective under oxidative stress conditions resulting in oxidised or haem-free sGC refractory to traditional organic nitrate therapies. Preliminary studies of cinaciguat in patients with acute decompensated heart failure show substantial improvements in haemodynamics and symptoms, whilst maintaining renal function.

show abstract

Section: Pgc Pathways and Nps: Nesiritide And Urodilatin/ Ularitidementioning

confidence: 99%

Role of guanylate cyclase modulators in decompensated heart failure

et al. 2009

View full text Add to dashboard Cite

show abstract

“…1). Within the 126 a.a. prohormone in the heart are four peptide hormones whose main biologic properties are blood pressure regulation and maintenance of plasma volume in animals [5][6][7][8][9][10][11] and humans [12][13][14][15][16]. These peptide hormones, numbered by their a.a. sequences beginning at the N-terminal end of the ANP prohormone, consist of the first 30 a.a. of the prohormone-that is, long acting natriuretic peptide (LANP), vessel dilator (a.a. 31-67), kaliuretic peptide (a.a. 79-98), and ANP (a.a. 99-126) [2,3].…”

Section: Cardiac Natriuretic Peptidesmentioning

confidence: 99%

“…On the contrary, vessel dilator markedly improves renal function when acute renal failure occurs [3,46]. The beneficial effects of vessel dilator last over 6 hours [12][13][14][15] …”

Section: Vessel Dilatormentioning

confidence: 99%

“…In persons with CHF, LANP at 0.1 μg/kg body weight/ min for 1 hour increases urine flow twofold and causes a 1.3-fold increased natriuresis with urine flow being blunted compared with its effects in healthy individuals [15] ( Table 1). The FE Na increased threefold secondary to LANP in patients with CHF [15].…”

Section: Lanpmentioning

confidence: 99%

“…Vessel dilator, however, enhanced sodium and FE Na more than kaliuretic peptide and more than ANP, nesiritide, ularitide, and LANP in persons with chronic CHF. Vessel dilator, LANP, and kaliuretic peptide-as opposed to ANP, ularitide, and nesiritide-have never caused a hypotensive episode when given to either healthy animals [6][7][8][9][10][11] or humans [12,13] or when given to humans with sodium and water retention [14][15][16].…”

Section: Kaliuretic Peptidementioning

confidence: 99%

See 2 more Smart Citations

Urodilatin: A better natriuretic peptide?

Vesely

2007

Curr Heart Fail Rep

Self Cite

View full text Add to dashboard Cite

The kidney natriuretic peptide urodilatin (ie, ularitide) decreases pulmonary capillary wedge pressure (PCWP) but does not cause diuresis in persons with congestive heart failure (CHF). Thirty-three percent of patients with CHF treated with 30 ng/kg/min ularitide develop hypotension with systolic blood pressures below 90 mmHg. Nesiritide and atrial natriuretic peptide lower PCWP and cause hypotension. They do not produce diuresis or natriuresis in patients with CHF. The best natriuretic peptide for treating CHF is the cardiac hormone vessel dilator which decreases PCWP and decreases systemic and pulmonary vascular resistance while simultaneously increasing cardiac output and cardiac index. What makes the vessel dilator markedly better than atrial natriuretic peptide, nesiritide, and ularitide for treatment of CHF is that it enhances sodium excretion fivefold and causes a fivefold enhanced diuresis in patients with CHF with its biologic effects lasting over 6 hours compared with less than 30 minutes for the above peptides.

show abstract

Natriuretic Hormones

Vesely

2013

Seldin and Giebisch's the Kidney

View full text Add to dashboard Cite

Comparison of vessel dilator and long-acting natriuretic peptide in the treatment of congestive heart failure

Cited by 17 publications

References 16 publications

Role of guanylate cyclase modulators in decompensated heart failure

Role of guanylate cyclase modulators in decompensated heart failure

Urodilatin: A better natriuretic peptide?

Natriuretic Hormones

Contact Info

Product

Resources

About